After the first detailed description of the delayed outward potassium current in squid axon by Hodgkin and Huxley (1952) it took electrophysiologists more than 20 years to realize that in addition to it several types of K+ currents can exist in the same cell and that they have a number of functions including modulation of cell excitability and modulation of integrating neuronal function. That as late as 1985 an international symposium on membrane control of cellular activity completely excluded K+ currents highlights the comparatively late interest of electrophysiologists in these ion currents. Moreover, our knowledge of the structure and function of K+ channels was very limited compared with what we know about Na2+ and Ca2+ channels and the acetylcholine receptor. One major reason has been the lack of suitable ligands that act on K+ channels with high affinity and selectivity such as tetrodotoxin on Na+ channels, dihydropyridines on one type of Ca2+ channels and α-bungarotoxin on nicotinic acetylcholine receptors. This has now profoundly changed mainly due to the development of the patch-clamp recording technique by Neher and Sakmann (Hamill et al. 1981), giving the tool to differentiate between an increasing number of receptor- and/or voltage-operated ion channels. Particularly the K+ channels have now mushroomed into a large, branching family of at least 11 members (Cook 1988). The dilemma is now that cell membranes, not only excitable ones, are equipped with a variety of K+ channels differing in their gating properties, which often complicates the interpretation of whole-cell K+ currents and their modulation by drugs.